African Trypanosomiasis is a systemic parasitic disease, which is caused by a protozoan Trypanosoma brucei and is transmitted to humans and animals by the bite of the tsetse flies which obtained the infection from humans and animals. Also known as African Sleeping Sickness, it is one of the most significant and abandoned tropical infections. Discovered in Africa during the period of 1894 – 1910, African Trypanosomiasis was identified by Sir David Bruce, Joseph Everett Dutton, Aldo Castellani, J.W.W. Stephens and H.B. Phantham. This infection occurs in two forms, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense.
“During the period of 1894 – 1910, the cause of the sleeping sickness in humans and cattle was discovered. David Bruce identified trypanosomes in the blood of affected cattle and established that healthy game animals were host reservoirs of the disease. Trypanosoma brucei was identified in 1899 and in 1902 Joseph Everett Dutton along with Robert Ford were first to identify Trypanosoma brucei gambiense in a European patient. In 1903, working along with Bruce, Aldo Castellani identified trypanosomes in the blood and cerebrospinal fluid of a patient with sleeping sickness. In 1910, J.W.W. Stephens and H.B. Phantham first described Trypanosoma brucei rhodesiense (3).”
Trypanosoma brucei is the protozoan that causes West African Sleeping Sickness and East African Sleeping Sickness. T. brucei has antigentic variations. Thus, by the time the body builds up an immune response against this pathogen, the pathogen has already altered its antigens and is unaffected by the antibodies (2). West African Sleeping Sickness or T. brucei gambiense, the more chronic of the two, is found in central and western Africa. This chronic condition can extend in a passive phase for months or years before symptoms emerge (4). Humans are the main reservoir for the T. brucei gambiense but can also be found in domestic animals. East African Sleeping Sickness or T. brucei rhodesiense is the acute form of the disease. It is found in southern and eastern Africa including Uganda, Kenya, Tanzania, Malawi, Ethiopia, Zaire, Zimbabwe, and Botswana. This acute condition shows signs and symptoms rather rapidly. Wild game animals and cattle are the main reservoir of T. brucei rhodesiense.
Both types of the infection are transmitted to humans and animals by the bite of the tsetse fly. The tsetse fly injects metacyclic trypomastigotes into the skin tissue of the mammalian host. The parasites enter the lymphatic system and pass into the blood stream. The trypomastigotes multiply by binary fission in various body fluids. Trypomastigotes then travel in the blood stream. The fly takes a blood meal from the mammalian host and trypomastigotes are ingested into the fly. Once inside the midgut of the fly the trypomastigotes transform into procyclic trypomastigotes and multiply by binary fission. The procyclic trypomastigotes then leave the midgut and transform into epimastigotes. The epimastigotes multiply in the salivary gland of the fly and transform into metacyclic trypomastigotes ready to be injected into another mammal (3).
West African Sleeping Sickness is usually found in Western and Central African forests, in areas of thick shrubbery and trees by rivers and waterholes. Risk of infection increases with the number of times a person is bitten by the tsetse fly. Thus, tourists are not at great risk for contracting West African trypanosomiasis unless they are traveling and spending long periods of time in rural areas of Western and Central Africa. East African Sleeping Sickness is usually found in woodland and savannah areas away from human habitation. Tourists, hunters, game wardens, and other persons working or visiting game parks in East and Central Africa are at greatest risk for illness.
Symptoms of West African Sleeping Sickness occur within months to years after getting an infected tsetse fly bite, while symptoms of the East African Sleeping Sickness begin within one to four weeks. Once painfully bitten, the infected bite mark develops into a red sore, a chancre. These are the local symptoms. The first stage or hemolymphatic stage of disease includes fever, rash, swelling around the eye and hands, severe headaches, extreme fatigue, aching muscles and joints. Swollen lymph nodes on the back of your neck, Winterbottom's sign, may develop in the West African Sleeping Sickness. Some people develop a skin rash with the East African Sleeping Sickness. Weight loss occurs as the illness progresses. The second stage or the encephalitic stage of the disease includes confusion, personality changes, slurred speech, irritability, loss of concentration, seizures, and difficulty in walking and talking occurs when infection has invaded the central nervous system. These symptoms become worse as the illness progresses. Sleeping for long periods of the day and having insomnia at night is a common symptom. If left untreated, infection becomes worse and death will occur within several months to years after infection (West African Sleeping Sickness) or several weeks or months after infection (East African Sleeping Sickness)(3,5).
Treatment for this disease depends on the form of infection and the stage on infection. Drugs used in the first hemolymphatic stage of West African Sleeping Sickness and East African Sleeping Sickness are pentamidine and suramin respectively. “Pentamidine was first used in 1940 and is administered intramuscularly. It interferes with the action and synthesis of polyamines and selective inhibition of parasite plasma membrane Ca2+-Mg2+-ATPase and Ca2+ transport. Suramin was first used in the early 1920’s and is administered through an i.v.. It inhibits the acute phase protein stimulation, mediated by impairment of receptor function and/or signal transduction. Until recently melarsoprol, a compound containing arsenic, was the only treatment readily available for the second encephalitic stage of both forms of the disease. Melarsoprol was first used in 1949 and is administered through and i.v.. It acts on trypanothione, a trypanosome molecule which maintains an intracellular reducing environment. Other drugs used in the second encephalitic stage of the West African Sleeping Sickness and East African Sleeping Sickness are include elfornithine and nifurtimox respectively. Elfornithine was first used in 1981 and is administered through an i.v.. It inhibits ornithine decarboxlyase, the key enzyme in polyamine biosynthesis. Nifurtimox was first used in 1977 and is administered orally. It interferes with trypanothione metabolism(3).”
In conclusion, African trypanosomiasis is a very serious disease with many questions still to be answered. It can not be prevented by any vaccination or drug. Thus, to help avoid exposure to the disease, try to prevent being bitten by the tsetse fly. Some of the preventive measures that should be taken include: “wearing long-sleeved shirts and pants made of thick material; wearing khaki or olive colored clothing because the tsetse fly is attracted to bright colors and very dark colors; using bed netting when sleeping; inspecting vehicles for tsetse flies before entering; not riding in the back of jeeps, pickup trucks or other open vehicles because the tsetse fly is attracted to the dust that moving vehicles and wild animals create; avoiding bushes because the tsetse fly is less active during the hottest period of the day and it rests in bushes but will bite if disturbed (1).”

Questions and Answers

Q. Can African Sleeping Sickness spread from human to human?
A. I think African Sleeping Sickness can be spread from human to human, if the body fluids of an infected person come in contact with the body fluids of the healthy person. If the healthy person becomes infected, this would be a start in proving that this disease can be spread from human to human.

Q. How does the tsetse fly know which humans and animals have the trypomastigotes in their blood stream when it comes to take a blood meal?
A. I think the there is something in the injected metacyclic trypomastigotes that alerts the fly that it can take a blood meal from this certain animal or human.

Works Cited

1. African Trypanosomiasis (African Sleeping Sickness). Travel Medicine/University of Virginia Health system Web site. Available at: http://www.healthsystem.virginia.edu/uvahealth/adult_travel/african.cfm. Accessed February 23, 2007.
2. Frank, Steven A.“A model for the sequential dominance of antigenic variants in African trypanosome infections.”The Royal Society 1999;226;1397-1401.
3. Kennedy, Peter G.E.“Human African trypanosomiasis of the CNS: current issues and challenges.”J. Clinical Investigation 2004;113;496-504.
4. Steverding, Dietmar.“A new initiative for the development of new diagnostic tests for human African trypanosomiasis” Kinetoplastid Biology and Disease 2006, 5:1
5. Stich A, Abel P, Krishna S.“Human African trypanosomiasis”BMJ 2002;325;203-06.